【摘要】：目的觀察乙酰輔酶A羧化酶(ACC)對Th17細(xì)胞分化的調(diào)控在急性哮喘小鼠模型發(fā)病機(jī)制中的作用。方法將24只雌性C57BL/6小鼠隨機(jī)分為正常對照組、哮喘組、DMSO對照組和ACC抑制劑組,每組6只。哮喘組、DMSO對照組和ACC抑制劑組予以卵清蛋白(OVA)致敏、激發(fā)建立急性哮喘模型,正常對照組對應(yīng)給予等體積的磷酸鹽緩沖液(PBS)處理。其中ACC抑制劑組每周2次給予腹腔注射ACC特異性抑制劑TOFA溶液(先溶于DMSO,后以PBS稀釋)處理,DMSO對照組對應(yīng)給予等濃度DMSO溶液處理。24 d后處死小鼠,收集肺組織和血清樣本。肺組織HE染色觀察小鼠肺組織炎性細(xì)胞浸潤情況,ELISA法檢測血清總IgE濃度,流式細(xì)胞術(shù)檢測肺組織Th17細(xì)胞在CD4~+T細(xì)胞中所占的百分率。結(jié)果哮喘組、DMSO對照組、ACC抑制劑組小鼠肺組織炎性細(xì)胞浸潤均較正常對照組顯著增加(3.50±0.14、3.47±0.08、2.07±0.20比0.50±0.17,均P0.001),DMSO對照組與哮喘組差異無統(tǒng)計(jì)學(xué)意義(P0.05),ACC抑制劑組較哮喘組顯著下降(P0.001)。哮喘組、DMSO對照組、ACC抑制劑組小鼠血清總IgE濃度均較正常對照組顯著升高[(5 680.40±831.40)ng/ml、(5 624.79±365.50)ng/ml、(2028.95±134.60)ng/ml比(400.52±57.13)ng/ml,均P0.008],且DMSO對照組與哮喘組差異無統(tǒng)計(jì)學(xué)意義(P0.05),ACC抑制劑組顯著低于哮喘組(P0.008)。哮喘組、DMSO對照組、ACC抑制劑組小鼠肺組織Th17細(xì)胞在CD4~+T細(xì)胞中所占百分率均較正常對照組明顯增高[(2.01±0.12)%、(1.95±0.16)%、(0.82±0.04)%比(0.59±0.03)%,均P0.008],DMSO對照組與哮喘組差異無統(tǒng)計(jì)學(xué)意義(P0.05),ACC抑制劑組較哮喘組顯著降低(P0.008)。結(jié)論抑制ACC后,OVA誘導(dǎo)的哮喘小鼠氣道炎癥顯著減輕,同時(shí)肺組織中Th17細(xì)胞減少,血清總IgE濃度下降,提示ACC可通過促進(jìn)Th17細(xì)胞分化參與哮喘的發(fā)病。
[Abstract]:Objective to investigate the effect of acetyl coA carboxylase (ACC) on the differentiation of Th17 cells in acute asthmatic mice. Methods 24 female C57BL/6 mice were randomly divided into normal control group, asthma group, DMSO control group and ACC inhibitor group. Asthma group, DMSO control group and ACC inhibitor group were sensitized with ovalbumin (OVA) to induce acute asthma model. The normal control group should be treated with the same volume of phosphate buffer (PBS). The ACC inhibitor group was treated by intraperitoneal injection of ACC specific inhibitor TOFA solution (dissolved in DMSO, and diluted with PBS) twice a week, and the DMSO control group was treated with DMSO solution of the same concentration. The mice were killed 24 days later, lung tissue and serum samples were collected. The infiltration of inflammatory cells in lung tissue was observed by HE staining, the total IgE concentration was detected by ELISA method, and the percentage of Th17 cells in CD4~ T cells was detected by flow cytometry. Results the infiltration of inflammatory cells in lung tissue in asthmatic group, DMSO control group and ACC inhibitor group was significantly higher than that in normal control group (3.50 鹵0.14 鹵3.47 鹵0.08 鹵2.07 鹵0.20 vs 0.50 鹵0.17). There was no significant difference between P0.001), DMSO control group and asthma group (P0.05). The serum total IgE levels in asthma group, DMSO control group and ACC inhibitor group were significantly higher than those in normal control group [(5 680.40 鹵831.40) ng/ml, (5 624.79 鹵365.50) ng/ml vs (400.52 鹵57.13) ng/ml, P 0.008], and there was no significant difference between DMSO control group and asthma group (P0.05).), ACC inhibitor group was significantly lower than asthma group (P0.008). The percentage of Th17 cells in lung tissue of asthma group, DMSO control group and ACC inhibitor group was significantly higher than that of normal control group [(2.01 鹵0.12)%, (1.95 鹵0.16)%, (0.82 鹵0.04)% vs (0.59 鹵0.03)%, P 0.008]. There was no significant difference between DMSO control group and asthma group (P0.05). Conclusion after inhibiting ACC, the airway inflammation induced by OVA in asthmatic mice was significantly alleviated, while the Th17 cells in lung tissue decreased, and the serum total IgE concentration decreased, suggesting that ACC may play a role in the pathogenesis of asthma by promoting the differentiation of Th17 cells.
【作者單位】： 武漢大學(xué)中南醫(yī)院呼吸內(nèi)科;
【基金】：國家自然科學(xué)基金(81072684)
【分類號(hào)】：R562.25

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